Differential diagnosis and treatment edema. Tactics gp

Protein deficiency
Edema and hypoalbuminemia with protein deficiency related. Edema occur when protein or complete starvation with the free fluid intake. In this case, the swelling may appear on the 3-5th day.In the differential diagnosis is of great importance to the construction of a patient survey of a food diary, as well as the presence of hypoalbuminemia in the absence of proteinuria. Edema are symmetrical. Often placed on the feet. Normalization of supply or intravenous drip in severe cases albumin accompanied by cupping edema. Effect of furosemide is low and increases only after infusion of albumin.
Enteropathy with increased protein loss.
Primary exudative enteropathy characterized by increased protein loss through the ectatic lymphatic vessels of the mucous membrane of the small intestine.
The main clinical manifestations:
- Expressed massive gipoproteinemicheskie often asymmetrical swelling;
- Swelling appear on the legs, arms, face, back;
- Sometimes anasarca;- It soon developed ascites and hydrothorax;
- Diarrhea appears to edema, often at the same time with them.
-Chair without mucus and blood;
- Patients concerned about abdominal pain, polifekaliya, constant bloating, rumbling, increased flatulence;
- In secondary exudative enteropathy leading signs
- increasing protein deficiency with a significant reduction in body weight, edema
- ascites syndrome, degenerative changes in all organs and body systems.
Hyperaldosteronism
Aldosteronism is common in clinical practice and is mainly due to three main problems: the use of diuretics, heart failure, and nephrotic syndrome. In this case, referred to as secondary hyperaldosteronism. Funds are also Con syndrome caused by benign tumor of the adrenal gland (aldosteronoma) with overproduction of aldosterone. In this case, there is primary aldosteronism. Removal of the tumor followed by cupping clinic disease.In the diagnosis of hyperaldosteronism is used to determine the level of aldosterone levels. When taking blood lying aldosterone concentration in normal is 8-172, with a fence in a standing position - 30-355 mg / ml.In primary hyperaldosteronism aldosterone concentration in the blood exceeds the normal of 5-10.
Marked sodium and water retention, increased potassium excretion in the urine. Edema are symmetrical. Swollen face, and limbs. Often develop hypertension.Unlike primary hyperaldosteronism secondary does not lead to the development of hypertensive syndrome. Much less pronounced edema (face pastosity, fingers and toes). Hyperaldosteronism is not an independent cause of anasarca, but pronounced swelling, such as nephrotic syndrome or chronic heart failure occur, usually with symptoms of secondary hyperaldosteronism. This is due to many reasons. Chief among these are the use of loop diuretics to control edema, with the development of hyponatremia, the formation of hypovolemia (nephrotic syndrome), circulatory hypoxia (chronic heart failure). They have stimulated renin secretion, which activates the conversion of angiotensinogen to angiotensin I, which leads to increased concentrations of angiotensin II and aldosterone. Aldosterone secretion is also enhanced directly at the impact of these factors.When taking diuretics, especially loop (furosemide, torasemide, ethacrynic acid), there giponatrioz, is a potent stimulus of aldosterone secretion. Therefore, a daily intake of furosemide in the same dose followed by a gradual decrease in urine output, despite the lack of complete relief phenomena overhydration. When psevdosindrome Barttera major pathogenetic link developing changes due to prolonged abuse of furosemide is hyperaldosteronism.